| 6. |
- Andersson, Anneli, 1992-, et al.
(författare)
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Genetic overlap between ADHD and externalizing, internalizing and neurodevelopmental disorder symptoms : a systematic review and meta-analysis
- 2018
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 48:6, s. 455-456
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Attention-Deficit/Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder (Wilens, Biederman & Spencer 2002) and affects approximately 5% of children (Polanczyk, de Lima, Horta, Biederman & Rohde 2007). About half of those diagnosed in childhood continue to have the diagnosis and symptoms in adulthood (Kessler et al. 2006). The co-occurrence of ADHD with other psychiatric disorder symptoms (Burt et al. 2001; Cole et al. 2009; Polderman et al. 2014) has been suggested to be partly explained by a shared genetic vulnerability (Polderman et al. 2014). However, the strength of the genetic overlap is currently unclear. Also, no study has examined whether the genetic correlations differs between age groups (childhood versus adulthood), by rater (self-report, other informant, combined (parent-teacher, parent-twin, teacher-twin)), or by type of psychiatric disorder symptoms (externalizing, internalizing, neu-rodevelopmental). To address this gap, we conducted a systematic literature search to identify relevant twin studies, in PubMed, PsycINFO, and EMBASE. A total of 31 articles were identified and included in the present study. The pooled estimates showed that the comorbidity between ADHD and diverse psychiatric disorder symptoms were explained by shared genetic effectsrg= 0.50 (0.43–0.56). A similar shared genetic overlap between ADHD and psychiatric disorder symptoms was observed in both childhood rg= 0.51(0.42–0.61) and adulthood rg= 0.47 (0.40–0.53). Similar results werealso found for self-reports rg= 0.49 (0.42–0.55), other informants rg= 0.50 (0.40–0.60), and combined raters rg= 0.51 (0.30–0.69). Further, the strength of the genetic correlations of ADHD with the externalizing rg= 0.49 (0.39–0.59), internalizing rg= 0.55 (0.40–0.68) and neurodevelopmental rg= 0.47 (0.40–0.53) spectrums were similar in magnitude. These findings emphasize the presence of a shared genetic liability between ADHD and externalizing, internalizing and neurodevelopmental disorder symptoms, independent of age and rater.ReferencesBurt, S. A., Krueger, R. F., McGue, M., Iacono, W. G. (2001).Sources of covariation among attention-deficit/hyperactivity disorder,oppositional defiant disorder, and conduct disorder: the importance ofshared environment.Journal of Abnormal Psychology, 4, 516–525.Cole, J., Ball, H. A., Martin, N. C., Scourfield, J., McGuffin, P.(2009). Genetic overlap between measures of hyperactivity/inatten-tion and mood in children and adolescents.J Am Acad Child AdolescPsychiatry48, 1094–1101.Kessler, R. C., Adler, L., Barkley, R., Biederman, J., Conners, C.K., Demler, O., Faraone, S. V., Greenhill, L. L., Howes, M. J., Secnik,K., Spencer, T., Ustun, T. B., Walters, E. E., Zaslavsky, A. M. (2006).The prevalence and correlates of adult ADHD in the United States:results from the National Comorbidity Survey Replication.Am JPsychiatry, 163, 716–723.Polanczyk, G., de Lima, M. S., Horta, B. L., Biederman, J., Rohde,L. A. (2007). The worldwide prevalence of ADHD: a systematicreview and metaregression analysis.Am J Psychiatry, 164, 942-8.Polderman, T. J., Hoekstra, R. A., Posthuma, D., Larsson, H.(2014). The co-occurrence of autistic and ADHD dimensions inadults: an etiological study in 17,770 twins.Transl Psychiatry2014;4: e435.Wilens, T. E., Biederman, J., Spencer, T. J. (2002). Attentiondeficit/hyperactivity disorder across the lifespan.Annual Review Med53:113–131.
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| 8. |
- Baker, Laura, et al.
(författare)
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The Relationship between IQ and PM2.5 : Findings from the University of Southern California Twin Study
- 2016
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 46:6, s. 772-773
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Tidskriftsartikel (refereegranskat)abstract
- We examined the longitudinal relationship between IQ and fine particulate matter (\2.5lm aerodynamic diameters; PM2.5) exposure in urban-dwelling children, using prospective longitudinal data from the USC Twin Study of Risk Factors for Antisocial Behavior (RFAB; Baker et al. 2013). Residential addresses were collected via selfreports. Verbal and Performance IQ during childhood (age 9–10) and young adulthood (age 19–20) were evaluated by the Wechsler Abbreviated Intelligence Scale (Wechsler, 1999) using four subtests: VIQ=Vocabulary Similarities; PIQ=Block Design Matrices. Based on residential addresses and spatiotemporal generalized additive model of local monitoring data for PM2.5, we estimated 1-year average exposure before each assessment. A three-level mixed effects model regressing IQ scores at each assessment on time-varying air pollution exposures, accounting for both within-family (random intercepts) and within-individual (random slopes) was used. PM2.5 exposure had significant adverse effects on PIQ (95 % CI of b:-7.29 to-1.01, p\.05) but not VIQ (95 % CI of b:-4.50 to-1.96). Adverse effects of PM2.5 exposure remained significant after adjusting for age, family SES, sex, race/ethnicity, parental cognitive abilities, neighborhood SES, neighborhood quality and neighborhood greenness; the association was still significant after further adjusting for traffic distance (300 m), temperature, humidity and annual NOx. PM2.5 exposure confers stronger adverse effects on PIQ in low SES families, males, and during pre-adolescence. Our findings reveal social disparities and sexual dimorphism in the adverse PM2.5 exposure effects on PIQ. Baker, L., Tuvblad, C., Wang, P., Gomez, K., Bezdjian, S., Niv, S., & Raine, A. (2013). The Southern California Twin Register at the University of Southern California: III. Twin Research and Human Genetics, 16(1), 336–343; Wechsler, D. (1999). Wechsler Abbreviated Scale of Intelligence (WASI). San Antonio, Texas: Harcourt Assessment.
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